Brain damage or dementia?

The nosological status of alcohol-related dementia as a distinct mental disorder remains hotly contested when interpreting the findings from studies of alcohol-related neuropathology and pathophysiology. Alcohol-induced brain injury is a consequence of direct neurotoxicity, oxidative stress, excitotoxicity from alcohol withdrawal, apoptosis, disruption of neurogenesis and mitochondrial damage. It is also further compounded by neuropathological changes typical of WKS, that can also accompany alcohol-related dementia. The direct effects of alcohol toxicity result in a continuum of cognitive dysfunction and behavioural change. These changes vary from less severe uncomplicated alcohol-induced brain injuries to those that are more severe and are complicated by nutritional deficiencies.Reference Savage, Svanberg, Withall, Draper and Bowden⁵ Neuroimaging and neuropathology studies indicate that the cardinal feature of alcohol-induced brain injury is a reduction in white matter within the frontal cortex, which is responsible for the disruption of the fronto-cerebellar circuit.Reference Savage, Svanberg, Withall, Draper and Bowden⁵

The neuropsychological profile of alcohol-related dementia has not been as well studied, but there is evidence that in comparison with Alzheimer's disease, language impairment is unlikely; with better performance on semantic tasks and on verbal memory recognition, but worse performance on visuospatial tasks.Reference Ridley, Draper and Withall⁴ However, as many also have features of WKS, there is often profound anterograde amnesia, impaired recall of past events and impaired executive functioning.Reference Ridley, Draper and Withall⁴

A UK cohort study of people with a mean age of 56 found that drinking above 32 UK units of alcohol per week was associated with greater global impairment in cognitive function, as well as in memory and executive function 10 years later.Reference Sabia, Elbaz, Britton, Bell, Dugravot and Shipley⁶ These global changes in cognitive function go beyond the neuropsychological profile of amnestic syndrome, which does not characteristically affect visuospatial function. There is also evidence for some degree of improvement in both white matter changes and neuropsychological impairment following abstinence in people with alcohol-related dementia.Reference Bartsch, Homola, Biller, Smith, Weijers and Wiesbeck⁷

The clinical presentation of alcohol-related dementia brings us closer to defining a mental disorder with a better defined neuropsychological profile. Although Oslin et al refined the diagnostic criteria to improve specificity by including measures of duration and severity of alcohol consumption, excluding characteristic features of Alzheimer's disease and vascular dementia and linking dementia with a minimum abstinence time before onset,Reference Oslin, Atkinson, Smith and Hendrie⁸ these criteria have yet to be validated in methodologically sound prospective studies.Reference Ridley, Draper and Withall⁴

Challenges and solutions

There remains a need to further explore the extent to which alcohol misuse can exacerbate primary degenerative and vascular dementias, traumatic brain injury and alcohol-related brain damage from other mechanisms such as other substance misuse and other physical disorders affecting brain function. There is also a dearth of evidence around the role of drug treatment in alcohol-related dementia, including the treatment of behavioural and psychological symptoms.

In 1990, alcohol ranked as the sixteenth leading cause of morbidity in England for the 50–69 age group. In 2013, it became the sixth leading cause.Reference Ilomaki, Jokanovic, Tan and Lonnroos⁹ At a public health level, there are mixed reports about the role of alcohol consumption and the development of dementia. An overview of systematic reviews of epidemiological studies predominantly involving participants aged 60 years and over concluded that light-to-moderate alcohol consumption might reduce the risk of Alzheimer's disease whereas heavy or excessive consumption did not affect the risk.¹⁰ However, a recent prospective study of people with a mean age of 43 at baseline followed up for 30 years found evidence of cognitive decline and hippocampal atrophy even with moderate alcohol consumption.Reference Topiwala, Allan, Valkanova, Zsoldos, Filippini and Sexton¹¹

The potential for reversibility has considerable implications for early intervention within addiction and old age psychiatry services. An increasing focus in the community on the prevention of dementia might provide another incentive for the early detection of alcohol-related dementia. Encouraging engagement with addiction services enables a smooth passage to the provision of cognitive rehabilitation interventions.Reference Wilson, Halsey, Macpherson, Billington, Hill and Johnson¹² With alcohol-related dementia displaying an identifiable neuropsychological profile, there is a need to incorporate wider neuropsychological testing and explore problems that distinguish frontal-lobe-mediated personality change from other features of alcohol dependence such as withdrawal and intoxication.

Given the presence of such cognitive impairment at younger ages, routine cognitive testing within addiction services would help to guide the primary and secondary prevention of alcohol-related dementia. This should also be mirrored by the provision of screening, brief intervention and referral for treatment in mainstream mental health services.

We need to address service provision and establish parity of esteem for alcohol-related dementia with alcoholic-related physical disorders such as alcohol-related liver disease; however, this cannot happen unless we tackle the broader issue of help-seeking, overcoming stigma and improving access to services. Against the background of a growing population of older people with alcohol misuse, no time can be lost to watchful waiting.